Serologic and Immunologic Responses in Chronic Fatigue Syndrome with Emphasis on the Epstein-Barr Virus

Jones, James F.

doi:10.1093/clinids/13.supplement_1.s26

Cited by 24 publications

(8 citation statements)

References 26 publications

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“…A large number of immune abnormalities, including cytokine production in CFS, have been reported (Buchwald & Komaroff, 1991, Gupta & Vayuvegula, 1991, Gupta, 1992, Jone, 1991, Kalimas et al, 1990, Lloyd et al, 1989, Straus et al, 1989. The published data on cytokine levels are contradictory (Cheney et al, 1989, Lever et al, 1988, Straus et al, 1989Lloyd et al, 1994, Linde et al, 1992.…”

Section: Introductionmentioning

confidence: 99%

Cytokine production by adherent and non-adherent mononuclear cells in chronic fatigue syndrome

Gupta

Aggarwal

See

et al. 1997

Journal of Psychiatric Research

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Summary--lt has been suggested that cytokines play a role in certain clinical manifestations of chronic fatigue syndrome (CFS). In this study adherent (monocytes) and non-adherent (lymphocytes) mononuclear cells were stimulated in the presence or absence of phytohemagglutinin (PHA) or lipopolysaccharide (LPS), respectively, and supernatants were assayed for IL-6, TNF-~, and IL-10 by ELISA. IL-6 was also measured at the mRNA level by polymerase chain reaction. The levels of spontaneously (unstimulated) produced TNF-.7 by non-adherent lymphocytes and spontaneously produced IL-6 by both adherent monocytes and non-adherent lymphocytes were significantly increased as compared to simultaneously studied matched controls. The abnormality of IL-6 was also observed at mRNA level. In contrast, spontaneously produced IL-10 by both adherent and non-adherent cells and by PHA-activated non-adherent cells were decreased. This preliminary study suggests that an aberrant production of cytokines in CFS may play a role in the pathogenesis and in some of the clinical manifestations of CFS. ,<) 1997 Elsevier Science Ltd.

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Section: Introductionmentioning

confidence: 99%

Cytokine production by adherent and non-adherent mononuclear cells in chronic fatigue syndrome

Gupta

Aggarwal

See

et al. 1997

Journal of Psychiatric Research

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“…Peterson, 1995). In CFS patients, immune disturbances have also been clinically reported (Aoki et al, 1993;Ojo-Amaize et al, 1994;Buchwald and Komaroff, 1991;Caligiuri et al, 1987;Cannon et al, 1997;Jones, 1991). In one study, CFS patients were treated with L-carnitine; improvement was related to symptom severity at the time the treatment began (Plioplys and Plioplys, 1997).…”

Section: Role For Mitochondrial Dysfunction In Chronic Fatigue Syndromementioning

confidence: 98%

Mitochondria in Pathogenesis

Lemasters¹,

Nieminen²

2002

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Preface Surprisingly, the mitochondrion has emerged as a center of attention in pathophysiology, generating both excitement and controversy. Old controversies concerning the mechanism of mitochondrial energy transduction subsided with the acceptance of Peter Mitchell's hypothesis of oxidative phosphorylation, first proposed in 1961. The chemiosmotic hypothesis elegantly described how mitochondrial respiration creates an electrochemical gradient of protons across the mitochondrial inner membrane, which in turn drives ATP synthesis through the mitochondrial ATP synthase. Tight coupling of this process requires that the mitochondrial inner membrane have an exceptionally low nonspecific permeability to protons and other charged solutions. In several pathological conditions, however, the mitochondrial permeability barrier fails, leading to cell death. Indeed, in programmed cell death (apoptosis) mitochondrial membrane failure may be a key signaling event. Moreover, the same respiratory processes that generate the proton electrochemical gradient driving oxidative phosphorylation may also lead to formation of toxic reactive oxygen species that cause cellular injury. Such oxygen radicals may contribute to the decline of bioenergetic capacity with advancing age.Among the organelles of animal cells, mitochondria are unique in that they contain their own DNA. The complete nucleotide sequence of human mtDNA is established, and it encodes genes for several hydrophobic subunits of complexes I, III, IV, and V, as well as genes for ribosomal proteins and tRNA. Mutations of mtDNA have wide-ranging consequences for mitochondrial respiration and bioenergetics. Because scores of mtDNA copies are maternally inherited, in contrast to the single maternal and paternal copies of nuclear DNA, mitochondrial diseases have unusual features of incomplete penetrance, delayed expression, and heterogeneous tissue involvement. In addition, possible links between mtDNA mutations, mitochondrial free radical generation, and several neurodegenerative diseases, including Huntington, Parkinson, and Alzheimer diseases, are under investigation by several laboratories.Toxic chemicals have long been known to disrupt mitochondrial metabolism and lead to cellular injury, but the mechanisms causing the injury are turning out to be more complex than expected. For instance, calcium, oxidant chemicals, ischemia/reperfusion, and a range of other agents promote onset of the mitochondrial permeability transition ix x Preface (MPT) in mitochondria from liver, heart, and other tissues, as first characterized by Hunter and Haworth in the mid-1970s. The significance of the MPT to pathophysiological processes, however, is only now being recognized. Besides involvement of the transition in necrotic cell death, new findings implicate it in apoptosis as well. Indeed, it may be the exceptional form of cell death that does not involve transition.This book attempts to provide an overview of recent major advances in the understanding of mitochondria's numerous roles in pathop...

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“…TGF-␤1 inhibits T-cell proliferation and suppresses some Th1 and Th2 cell-mediated autoimmune diseases (Kehrl et al, 1986;Holter et al, 1994;Mosmann and Sad, 1996;Bridoux et al, 1997). A large number of immune abnormalities, including cytokine production in CFS, have been reported (Klimas et al, 1990;Buchwald and Komaroff, 1991;Gupta and Vayuvegula, 1991;Gupta, 1992;Jone, 1991;Lloyed et al, 1989;Straus et al, 1989). Recent insights into autoimmune type disease have suggested a pivotal role for the pro-inflammatory cytokine tumor necrosis factor (TNF)-␣.…”

Section: Introductionmentioning

confidence: 99%

Effect of Kuibitang on lipopolysaccharide-induced cytokine production in peripheral blood mononuclear cells of chronic fatigue syndrome patients

Shin¹,

An²,

Cha³

et al. 2004

Journal of Ethnopharmacology

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Serologic and Immunologic Responses in Chronic Fatigue Syndrome with Emphasis on the Epstein-Barr Virus

Cited by 24 publications

References 26 publications

Cytokine production by adherent and non-adherent mononuclear cells in chronic fatigue syndrome

Cytokine production by adherent and non-adherent mononuclear cells in chronic fatigue syndrome

Mitochondria in Pathogenesis

Effect of Kuibitang on lipopolysaccharide-induced cytokine production in peripheral blood mononuclear cells of chronic fatigue syndrome patients

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